Jeng Mark Y, Ali Ibraheem, Ott Melanie
a Gladstone Institute of Virology and Immunology , San Francisco , CA , USA and.
b Department of Medicine , University of California , San Francisco , CA , USA.
Crit Rev Biochem Mol Biol. 2015;50(4):314-25. doi: 10.3109/10409238.2015.1061973. Epub 2015 Sep 2.
Over the past 15 years, protein acetylation has emerged as a globally important post-translational modification that fine-tunes major cellular processes in many life forms. This dynamic regulatory system is critical both for complex eukaryotic cells and for the viruses that infect them. HIV-1 accesses the host acetylation network by interacting with several key enzymes, thereby promoting infection at multiple steps during the viral life cycle. Inhibitors of host histone deacetylases and bromodomain-containing proteins are now being pursued as therapeutic strategies to enhance current antiretroviral treatment. As more acetylation-targeting compounds are reaching clinical trials, it is time to review the role of reversible protein acetylation in HIV-infected CD4(+) T cells.
在过去15年中，蛋白质乙酰化已成为一种在全球范围内重要的翻译后修饰，它对许多生命形式中的主要细胞过程进行微调。这种动态调节系统对于复杂的真核细胞以及感染它们的病毒都至关重要。HIV-1通过与几种关键酶相互作用进入宿主乙酰化网络，从而在病毒生命周期的多个步骤中促进感染。目前正在寻求宿主组蛋白脱乙酰酶和含溴结构域蛋白的抑制剂作为增强当前抗逆转录病毒治疗的治疗策略。随着越来越多的靶向乙酰化的化合物进入临床试验阶段，现在是时候回顾可逆蛋白质乙酰化在HIV感染的CD4(+) T细胞中的作用了。
